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British Journal of Anaesthesia, 1994, Vol. 72, No. 6 668-673
© 1994 The Board of Management and Trustees of the British Journal of Anaesthesia

research-article

Molecular actions of pentobarbitone on sodium channels in lipid bilayers: role of channel structure{dagger}

H. C. WARTENBERG, M.D.*, J. WANG, M.D.*, B. REHBERG, M.D.*, B. W. URBAN, PH.D and D. S. DUCH, PH.D.

Department of Anesthesiology and Physiology, Cornell University Medical School 1300 York Avenue, New York, NY 10021, U.S.A.
Departments of Anesthesiology and Physiology, Cornell University Medical College, New York and Klinik und Poliklinik für Anästhesiologie und spezielle Intensivmedizin, Rheinische Friedrich-Wilhelms-Universität Bonn Germany

Correspondence to D.S.D.

The molecular mechanisms by which anaesthetics interfere with neuronal function are controversial. We have examined the effects of pentobarbitone on muscle-derived (eel electroplax) sodium channels incorporated into planar bilayers under exactly the same experimental conditions that we used previously to study the anaesthetic modification of human brain channels. This technique allows examination of protein-mediated similarities and differences. Sodium channels from the electroplax (muscle-derived) of the electric eel were purified and reconstituted into planar lipid bilayers containing 4:1 phosphatidylethanolamine:phosphatidylcholine in the presence of batrachotoxin, a sodium channel activator. Pentobarbitone had similar voltage-independent blocking effects on sodium channels from eel electroplax and human brain, as demonstrated by similar dose-response curves (IC50=613 µmol litre–1). However, activation of sodium channels from eel electroplax, in contrast with human brain, was relatively insensitive to the concentration of pentobarbitone. The only significant effect was a -5.8-mV shift in the activation midpoint with pentobarbitone 680 µmvol litre–1. Therefore, differences in primary structures played no role in the observed voltage-independent block of channels by pentobarbitone, whereas subunits or other structural differences between sodium channels from eel electroplax and human brain must be responsible for the minimal effect of pentobarbitone on activation of muscle-derived sodium channels.

{dagger}Presented in part at the Annual Meeting of the American Society of Anesthesiologists, San Francisco, California, October, 1991.

Present address: Klinik und Poliklinik für Anästhesiologie und spezielle Intensivmedizin, Rheinische Friedrich-Wilhelms-Universität Bonn, Germany


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